An experimental study on the pathogenesis of gastroesophageal reflux after repair of diaphragmatic hernia

Gastroesophageal reflux (GER) is increasingly reported after surgical repair of congenital diaphragmatic hernia (CDH) and eventration. The aim of this study was to test the hypothesis that transdiaphragmatic pressure gradients are increased and that the antireflux barrier is weakened after plication of a previously paralyzed diaphragm.

Abdominal and esophageal pressures as well as lower esophageal sphincter pressures (LESP) and diaphragmatic pinchcock pressure (DPP) were measured before and after diaphragmatic plication in 16 rats in which the diaphragm had been previously eventrated by phrenic nerve section.

This maneuver increased the transdiaphragmatic inspiratory pressure gradient from 2.75 +/- 0.54 to 4.51 +/- 0.86 mm Hg (P < .05) by rising both the inspiratory (-2.02 +/- 0.39 v -3.11 +/- 0.92 mm Hg, P < .05) and the expiratory (1.47 +/- 0.87 v 0.51 +/- 0.41 mm Hg, P < .05) intrathoracic pressures. At the same time, the antireflux barrier was weakened because LESP decreased from 17.5 +/- 5.59 to 10.59 +/- 5.74 mm Hg (P < .05) and DPP tended to decrease from 13.57 +/- 8.67 to 6.07 +/- 1.72 mm Hg (ns).

Plication of the previously paralyzed diaphragm in the rat reinforces the GER driving forces while weakening the antireflux barrier. This may explain why reflux is frequent in children surviving repair of diaphragmatic hernia and eventration.